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      Relationship between blood lipid profiles and pancreatic islet β cell function in Chinese men and women with normal glucose tolerance: a cross-sectional study

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          Dyslipidemia is present in people with diabetes as well as subjects with normal glucose tolerance (NGT). The purpose of this study was to investigate the relationship between lipid profiles and β cell function in Chinese individuals with NGT but without history of diabetes or prediabetes.


          A total of 893 men and 1454 women aged 18–76 years living in Sichuan, China, who were not being treated with lipid-lowering drugs were enrolled in this study. Insulin sensitivity (IR) was evaluated using the homeostasis model assessment –IR (HOMA-IR), β-cell function was calculated by the following equation: ΔI30/ΔG30/ HOMA-IR (ΔI30/ΔG30: the ratio of incremental glucose and insulin 30 min after glucose intake). Multivariate linear regression analyses were performed to estimate the relationship between blood lipid and β cell function as standardized coefficients (β).


          β cell function decreased in men and women with increasing age. We found inverse relationships between β cell function and total cholesterol (TC) in men and women (β = −0.157 and −0.113, respectively, both p < 0.001), low-density lipoprotein–cholesterol (LDL-C; β = −0.130 and −0.068, respectively, both p < 0.001), TC/high-density lipoprotein–cholesterol (HDL-C) ratio (β = −0.084, p < 0.01 and −0.096, p < 0.001), and triglycerides (TG) (women only; β = −0.053, p < 0.05). However, β cell function was not associated with HDL-C in men or women (β = −0.034 and 0.000, respectively, both p > 0.05) or the TG/HDL-C ratio (β = −0.035 and −0.013, respectively, both p > 0.05). β cell function was significantly worse in males than in females in all age groups, except in subjects aged > 70 years.


          Dyslipidemia is associated with dysfunction of pancreatic β cells in subjects with NGT and this is particularly evident in people with elevated TC and LDL-C levels, especially males.

          Trial Registration Number

          #TR-CCH-Chi CTR-CCH-00000361

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          Most cited references 18

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          Fatty acid-induced beta cell apoptosis: a link between obesity and diabetes.

          Like obese humans, Zucker diabetic fatty (ZDF) rats exhibit early beta cell compensation for insulin resistance (4-fold beta cell hyperplasia) followed by decompensation (>50% loss of beta cells). In prediabetic and diabetic ZDF islets, apoptosis measured by DNA laddering is increased 3- and >7-fold, respectively, compared with lean ZDF controls. Ceramide, a fatty acid-containing messenger in cytokine-induced apoptosis, was significantly increased (P 1 mM) in prediabetic and diabetic ZDF rats; therefore, we cultured prediabetic islets in 1 mM FFA. DNA laddering rose to 19.6% vs. 4.6% in lean control islets, preceded by an 82% increase in ceramide. C2-Ceramide without FFA induced DNA laddering, but fumonisin B1, a ceramide synthetase inhibitor, completely blocked FFA-induced DNA laddering in cultured ZDF islets. [3H]Palmitate incorporation in [3H]ceramide in ZDF islets was twice that of controls, but [3H]palmitate oxidation was 77% less. Triacsin C, an inhibitor of fatty acyl-CoA synthetase, and troglitazone, an enhancer of FFA oxidation in ZDF islets, both blocked DNA laddering. These agents also reduced inducible nitric oxide (NO) synthase mRNA and NO production, which are involved in FFA-induced apoptosis. In ZDF obesity, beta cell apoptosis is induced by increased FFA via de novo ceramide formation and increased NO production.
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            Beta-cell ABCA1 influences insulin secretion, glucose homeostasis and response to thiazolidinedione treatment.

            Type 2 diabetes is characterized by both peripheral insulin resistance and reduced insulin secretion by beta-cells. The reasons for beta-cell dysfunction in this disease are incompletely understood but may include the accumulation of toxic lipids within this cell type. We examined the role of Abca1, a cellular cholesterol transporter, in cholesterol homeostasis and insulin secretion in beta-cells. Mice with specific inactivation of Abca1 in beta-cells had markedly impaired glucose tolerance and defective insulin secretion but normal insulin sensitivity. Islets isolated from these mice showed altered cholesterol homeostasis and impaired insulin secretion in vitro. We found that rosiglitazone, an activator of the peroxisome proliferator-activated receptor-gamma, which upregulates Abca1 in beta-cells, requires beta-cell Abca1 for its beneficial effects on glucose tolerance. These experiments establish a new role for Abca1 in beta-cell cholesterol homeostasis and insulin secretion, and suggest that cholesterol accumulation may contribute to beta-cell dysfunction in type 2 diabetes.
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              Direct effect of cholesterol on insulin secretion: a novel mechanism for pancreatic beta-cell dysfunction.

              Type 2 diabetes is often accompanied by abnormal blood lipid and lipoprotein levels, but most studies on the link between hyperlipidemia and diabetes have focused on free fatty acids (FFAs). In this study, we examined the relationship between cholesterol and insulin secretion from pancreatic beta-cells that is independent of the effects of FFAs. Several methods were used to modulate cholesterol levels in intact islets and cultured beta-cells, including a recently developed mouse model that exhibits elevated cholesterol but normal FFA levels. Acute and metabolic alteration of cholesterol was done using pharmacological reagents. We found a direct link between elevated serum cholesterol and reduced insulin secretion, with normal secretion restored by cholesterol depletion. We further demonstrate that excess cholesterol inhibits secretion by downregulation of metabolism through increased neuronal nitric oxide synthase dimerization. This direct effect of cholesterol on beta-cell metabolism opens a novel set of mechanisms that may contribute to beta-cell dysfunction and the onset of diabetes in obese patients.

                Author and article information

                BMC Public Health
                BMC Public Health
                BMC Public Health
                BioMed Central
                10 August 2012
                : 12
                : 634
                [1 ]Department of Endocrinology and Metabolism, West China Hospital of Sichuan University, Chengdu, 610041, People's Republic of China
                [2 ]Department of Endocrinology, West China Hospital, Sichuan University, 37 GuoXue Street, Chengdu, Sichuan, 610041, China
                Copyright ©2012 Zheng et al.; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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